POS0686 EFFECTIVENESS OF UPADACITINIB IN THE TREATMENT OF RHEUMATOID ARTHRITIS: ANALYSIS OF 6-MONTH REAL-WORLD DATA FROM THE UNITED RHEUMATOLOGY NORMALIZED INTEGRATED COMMUNITY EVIDENCE (UR-NICETM) DATABASE
Authors: A. Gibofsky, M. E. Pearson, A. Concoff, A. Shmagel, P. Zueger, Y. Song, L. Smith, G. C. Wright
Journal: Annals of the Rheumatic Diseases (2022)

Background The efficacy of upadacitinib (UPA), an oral Janus kinase inhibitor (JAKi), in the treatment of rheumatoid arthritis (RA) has been demonstrated in the phase 3 SELECT clinical trial program. 1–6 However, few real-world data have been reported to date. Objectives To assess the 6-month effectiveness of UPA in patients (pts) with RA initiating UPA treatment in clinical practice. Methods This observational study included US-based pts from the United Rheumatology Normalized Integrated Community Evidence (UR-NICE) database who initiated UPA 15 mg once daily from Aug 2019 to the data cut-off in Nov 2021. Pts with ≥6 months of baseline (BL) data before UPA initiation, and with Clinical Disease Activity Index (CDAI) score recorded at BL and 6 months (±45 days) after initiation, were included in the analysis. Effectiveness measures included CDAI score, Routine Assessment of Patient Index Data 3 (RAPID3), and Disease Activity Score in 28 joints based on C-reactive protein (DAS28-CRP); patient-reported outcomes (PROs) including Health Assessment Questionnaire-Disability Index (HAQ-DI), Pain, and Patient’s Global Assessment of Disease Activity (PtGA); and Physician’s Global Assessment of Disease Activity (PhGA). Subgroup analyses were conducted by prior tumor necrosis factor inhibitor (TNFi) and tofacitinib (TOFA) treatment history. Results 363 pts were included in the analysis and most were female (80.2%) (Table 1). 140 (39%) received UPA monotherapy and 223 (61%) received UPA plus conventional synthetic (cs) disease-modifying antirheumatic drugs (DMARDs). 83% of pts received prior csDMARDs, 72% prior biologics (TNFi 55%), and 41% JAKis (TOFA 39%). Overall, 46% (166/363), 23% (57/245), and 55% (95/173) of pts achieved LDA by CDAI, RAPID3, and DAS28-CRP, respectively, and 14% (51/363), 16% (39/245), and 36% (62/173) of pts achieved remission (REM) by CDAI, RAPID3, and DAS28-CRP, respectively. Results were similar regardless of prior TNFi or TOFA exposure (Figure 1). Improvements from BL were seen in PhGA and all PROs in the total population and all subgroups. Table 1. Demographic and baseline characteristics Parameter, n (%) Full analysis set Prior TNFi Prior TOFA (N=363) (n=199) (n=143) Female 291 (80.2) 156 (78.4) 119 (83.2) Age, years &lt;40 22 (6.1) 11 (5.5) 8 (5.6) 40–&lt;65 240 (66.1) 132 (66.3) 94 (65.7) ≥65 101 (27.8) 56 (28.1) 41 (28.7) Oral steroid use 185 (51.0) 103 (51.8) 83 (58.0) Parameter, mean (SD ) N Mean (SD ) n Mean (SD ) n Mean (SD ) Duration of RA, years 276 4.5 (3.1) 162 5.1 (3.0) 113 5.1 (2.9) Body mass index, kg/m 2 321 30.0 (6.9) 175 29.9 (6.6) 125 29.2 (6.7) Oral steroid dose (prednisone equivalent), mg/day 154 7.9 (6.9) 87 7.8 (6.5) 70 7.6 (6.1) Methotrexate dose, mg/week 119 18.3 (4.9) 74 17.8 (5.2) 37 18.2 (4.7) C-reactive protein, mg/L 228 9.6 (16.2) 132 9.4 (15.0) 90 11.3 (17.9) CDAI 363 21.2 (12.8) 199 22.1 (13.0) 143 21.7 (13.3) RAPID3 268 4.7 (2.1) 141 4.7 (2.2) 100 4.9 (2.1) DAS28-CRP 228 3.9 (1.3) 132 4.0 (1.4) 90 4.2 (1.3) HAQ-DI a 273 2.6 (2.1) 148 2.8 (2.2) 106 3.0 (2.2) Pain b 338 59.6 (26.6) 186 58.4 (27.2) 131 61.3 (25.1) PtGA b 363 54.1 (25.6) 199 54.7 (26.9) 143 55.9 (25.2) PhGA b 363 41.3 (26.0) 199 41.2 (24.8) 143 40.7 (26.8) a 0–10 visual analog scale. b 0–100 visual analog scale. SD, standard deviation. Conclusion In this study, almost half (46%) of pts treated with UPA achieved CDAI LDA at 6 months and 14% achieved CDAI REM. Improvements in all PROs and PhGA were observed. Effectiveness of UPA was not impacted by prior TNFi or TOFA exposure, supporting UPA as an effective treatment option in clinical practice, including in pts with prior exposure to advanced therapy. References [1]Burmester GR, et al. Lancet 2018;391:2503–12. [2]Smolen JS, et al. Lancet 2019;393:2303–11. [3]Fleischmann R, et al. Arthritis Rheumatol 2019;71:1788–800. [4]Genovese MC, et al. Lancet 2018;391:2513–24. [5]van Vollenhoven R, et al. Arthritis Rheumatol 2020;72:1607–20. [6]Rubbert-Roth A, et al. N Engl J Med 2020;383:1511–21. Acknowledgements AbbVie funded this study; contributed to its design; participated in data collection, analysis, and interpretation of the data; and participated in the writing, review, and approval of the abstract. AbbVie and the authors thank all study investigators for their contributions and the patients who participated in this study. No honoraria or payments were made for authorship. Medical writing support was provided by Laura Chalmers, PhD, of 2 the Nth (Cheshire, UK), and was funded by AbbVie. Disclosure of Interests Allan Gibofsky Shareholder of: AbbVie, Amgen, Johnson &amp; Johnson, and Pfizer (stocks), Consultant of: AbbVie, Celgene, Eli Lilly, Flexion, Pfizer, Relburn Pharma, and Samumed (consulting fees); and Gerson Lehrman Group (paid consultant with investment analysts), Mark E. Pearson Shareholder of: AbbVie (may own stock or options), Andrew Concoff Speakers bureau: Flexion Therapeutics and Exagen, Consultant of: Flexion Therapeutics and Exagen, Anna Shmagel Shareholder of: AbbVie (may own stock or options), Employee of: AbbVie, Patrick Zueger Shareholder of: AbbVie (may own stock or options), Employee of: AbbVie, Yanna Song Shareholder of: AbbVie (may own stock or options), Employee of: AbbVie, Lauren Smith Shareholder of: AbbVie (may own stock or options), Employee of: AbbVie, Grace C. Wright Speakers bureau: AbbVie, Amgen, Bristol-Myers Squibb, Eli Lilly, Exagen, Myriad Autoimmune, Novartis, Sanofi/Regeneron, UCB, and Vindico, Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Eli Lilly, Exagen, Gilead, Janssen, Myriad Autoimmune, Novartis, Pfizer, Sanofi/Regeneron, and UCB, Employee of: Association of Women in Rheumatology (President and Founder)